Are humans apes?

[Trolldor]

...Sexual reproduction is replication. The sperm and ovum have DNA copied from the original source - with mutations/errors.

[GenesForLife]

Until I get scientific papers in, I have something to chew on here

http://scienceblogs.com/evolgen/2007/01 ... romoso.php

This is an excerpt from the source.

Floating polymorphism for Robertsonian fusions is quite common, and in many cases apparently causes little or no reductiuon in fertility (examples from rodents, spiders, grasshoppers, bovids, cockroaches....). There is no clear pattern as to when fusions will result in nondisjunction vs when they won't, but fusion trivalents are more likely to be stable when the arms of the fusion are of similar length (there is a difference in arm length on our chromosome 2, but it isn't extreme) and crossovers are relatively distal (don't know if that is the case here) - the 14/21 fusion in humans is an example of very unequal arm lengths and it often missegregates, although people with this fusion still produce offspring and most are normal (5-10% of offspring are tri 21, presumably many more lost through spontaneous abortion, in addition to the other nondisjunction products). So fixation of the chromosome 2 fusion is unlikely to have required the very extreme circumstances you have outlined.

This paper may be of use when talking about deleterity of fusion events.

Abstract

Several authors have proposed that speciation frequently occurs when a population becomes fixed for one or more chromosomal rearrangements that reduce fitness when they are heterozygous. This hypothesis has little theoretical support because mutations that cause a large reduction in fitness can be fixed through drift only in small, inbred populations. Moreover, the effects of chromosomal rearrangements on fitness are unpredictable and vary significantly between plants and animals. I argue that rearrangements reduce gene flow more by suppressing recombination and extending the effects of linked isolation genes than by reducing fitness. This unorthodox perspective has significant implications for speciation models and for the outcomes of contact between neospecies and their progenitor(s).

http://www.sciencedirect.com/science?_o ... archtype=a

One more paper is here, suggesting it may be a common occurrence.

The occurrence of spontaneous Robertsonian fusion leading to 2n=39 chromosomes (NF=40) in the house mouse (Mus musculus domesticus) has been reported for the first time from Asia. 3 phenotypically normal female mice collected from 2 distantly located populations of India (Tripura and Calcutta) show centric fusion in somatic chromosomes between pairs 2 and 16, and 8 and 14 respectively. C-banding analysis revealed that the (sub) metacentric has been originated by fusion between the broken/eroded centromeres of 2 telocentric chromosomes.

http://www.springerlink.com/content/u56481606tu83u41/

Several possible mechanisms of Robertsonian fusions are discussed here

The Robertsonian (Rb) fusion, a chromosome rearrangement involving centric fusion of two acro-(telo)centric chromosomes to form a single metacentric, is one of the most frequent events in mammalian karyotype evolution. Since one of the functions of telomeres is to preserve chromosome integrity, a prerequisite for the formation of Rb fusions should be either telomere loss or telomere inactivation. Possible mechanisms underlying the formation of various types of Rb fusion are discussed here. For example, Rb fusion in wild mice involves complete loss of p-arm telomeres by chromosome breakage within minor satellite sequences. By contrast, interstitial telomeric sites are found in the pericentromeric regions of chromosomes originating from a number of vertebrate species, suggesting the occurrence of Rb-like fusion without loss of telomeres, a possibility consistent with some form of telomere inactivation. Finally, a recent study suggests that telomere shortening induced by the deletion of the telomerase RNA gene in the mouse germ-line leads to telomere loss and high frequencies of Rb fusion in mouse somatic cells. Thus, at least three mechanisms in mammalian cells lead to the formation of Rb fusions.

http://www.springerlink.com/content/3flwx2p74t1ajq9r/

[hackenslash]

Are you sure you want to do this, MM? The word 'quixotic' springs to mind, except that the particular windmill you are tilting at is rather well-versed in genetics. Frankly, you might as well go and argue about black holes with Stephen Hawking.

[Tigger]

Are you sure you want to do this, MM? The word 'quixotic' springs to mind, except that the particular windmill you are tilting at is rather well-versed in genetics. Frankly, you might as well go and argue about black holes with Stephen Hawking.

What a lovely and apt compliment for GFL.

[mistermack]

Are you sure you want to do this, MM? The word 'quixotic' springs to mind, except that the particular windmill you are tilting at is rather well-versed in genetics. Frankly, you might as well go and argue about black holes with Stephen Hawking.

I notice you've got nothing specific to say. You might as well stick that gem back up the cow's ass.
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[Tigger]

Are you sure you want to do this, MM? The word 'quixotic' springs to mind, except that the particular windmill you are tilting at is rather well-versed in genetics. Frankly, you might as well go and argue about black holes with Stephen Hawking.

I notice you've got nothing specific to say. You might as well stick that gem back up the cow's ass.
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Why have a dog?

[GenesForLife]

The only point where Mack may have a slight point to make is wrt the role of genes in fusion events, it isn't that genes per se that are involved, but loss of telomere function could theoretically end up producing fusion events, and this itself could be a consequence of a defunct telomerase enzyme. However, if one were to consider this factor as crucial to the enabling of the fusion event in the human lineage, we must be forced to ask why this was specific to just two chromosomes and not more widespread. At this juncture, the following paper may be of relevance

End-to-end associations of metaphase chromosomes have been observed in a variety of human tumors, ageing cells, and several chromosome instability syndromes. Since telomeres of tumor cells and ageing tissues are often reduced in length, it has been suggested that chromosome end associations may be due to loss of telomeric repeats. We report the molecular structure of telomeres of two human tumor cell lines with frequent end-to-end associations of metaphase chromosomes. These telomeres were shown to be severely reduced compared with most other human cells with functional telomeres. However, we also describe two cell lines with severely shortened telomeres that are not detectably compromised in their function. We suggest that telomeric length is not the only determinant of the fusigenic behavior of human telomeres in tumor cells.

http://www.springerlink.com/content/nk3286711704626h/

The bolded part is especially significant because it raises questions about mechanisms for end-to-end fusion behaviour in chromosomes that are independent of telomere length (which by the way is determined by telomerase activity and function, not least because hTERT, or Human Telomerase Reverse Transcriptase, the enzyme which generates the telomeres, has its own built in template) which would mean, if we were to assume a mutant telomerase enabled fusion event, would actually make that hypothesis dodgy.

The possible genetic link of telomerase in this case with chromosome fusion here is an unlikely hypothesis for the fusion event in human evolutionary history.

[JimC]

It seems to me that there are two sorts of fusion events, at least as far as their evolutionary import. One, which can occur fairly randomly in populations of various organisms (like wild mice mentioned in an earlier post), and may or may not cause some loss of fitness or reproductive activity in the individuals concerned. There are also, apparently, some examples of this on relatively rare occasions in humans.

The other type is exemplified by the fused chromosomes in the human lineage, which have become fixed in the population and become a normal feature of the karyotype of the species, and a clear difference to the others within their close relatives. I gather that this has also been observed in a number of other species which have diverged from an ancestral stock.

[GenesForLife]

It seems to me that there are two sorts of fusion events, at least as far as their evolutionary import. One, which can occur fairly randomly in populations of various organisms (like wild mice mentioned in an earlier post), and may or may not cause some loss of fitness or reproductive activity in the individuals concerned. There are also, apparently, some examples of this on relatively rare occasions in humans.

Just want to correct you there, the ones in the mice also referred to supernumerary chromosomes, so it very well could have been a gain in chromosome number by chromosome duplication in a lot of cases depending on the ancestral karyotype and fusion events in the rest.

[JimC]

It seems to me that there are two sorts of fusion events, at least as far as their evolutionary import. One, which can occur fairly randomly in populations of various organisms (like wild mice mentioned in an earlier post), and may or may not cause some loss of fitness or reproductive activity in the individuals concerned. There are also, apparently, some examples of this on relatively rare occasions in humans.

Just want to correct you there, the ones in the mice also referred to supernumerary chromosomes, so it very well could have been a gain in chromosome number by chromosome duplication in a lot of cases depending on the ancestral karyotype and fusion events in the rest.

Thanks, mate!

But whatever the cause of alterations to karyotype within a species (duplication or fusion), do you take my point that, on the one hand, we have these random variations within a species, and on the other (the human chimp thing), we have a clear and consistent difference between one branch of a monphyletic group and the remainder?

[GenesForLife]

It seems to me that there are two sorts of fusion events, at least as far as their evolutionary import. One, which can occur fairly randomly in populations of various organisms (like wild mice mentioned in an earlier post), and may or may not cause some loss of fitness or reproductive activity in the individuals concerned. There are also, apparently, some examples of this on relatively rare occasions in humans.

Just want to correct you there, the ones in the mice also referred to supernumerary chromosomes, so it very well could have been a gain in chromosome number by chromosome duplication in a lot of cases depending on the ancestral karyotype and fusion events in the rest.

Thanks, mate!

But whatever the cause of alterations to karyotype within a species (duplication or fusion), do you take my point that, on the one hand, we have these random variations within a species, and on the other (the human chimp thing), we have a clear and consistent difference between one branch of a monphyletic group and the remainder?

Erm, look, I do not think there is a strict demarcation as such, it may very well turn out that the karyotype gets to a mean with time, i.e, these populations of mice may end up having a stable number of chromosomes and a speciation event, in such a case, as long as there is a difference between the now-stabilized chromosome numbers between the descendent species and the ancestral species we'll have gotten examples for the second category that may have taken a path through the first category during the course of evolution.

[JimC]

It seems to me that there are two sorts of fusion events, at least as far as their evolutionary import. One, which can occur fairly randomly in populations of various organisms (like wild mice mentioned in an earlier post), and may or may not cause some loss of fitness or reproductive activity in the individuals concerned. There are also, apparently, some examples of this on relatively rare occasions in humans.

Just want to correct you there, the ones in the mice also referred to supernumerary chromosomes, so it very well could have been a gain in chromosome number by chromosome duplication in a lot of cases depending on the ancestral karyotype and fusion events in the rest.

Thanks, mate!

But whatever the cause of alterations to karyotype within a species (duplication or fusion), do you take my point that, on the one hand, we have these random variations within a species, and on the other (the human chimp thing), we have a clear and consistent difference between one branch of a monphyletic group and the remainder?

Erm, look, I do not think there is a strict demarcation as such, it may very well turn out that the karyotype gets to a mean with time, i.e, these populations of mice may end up having a stable number of chromosomes and a speciation event, in such a case, as long as there is a difference between the now-stabilized chromosome numbers between the descendent species and the ancestral species we'll have gotten examples for the second category that may have taken a path through the first category during the course of evolution.

Fair point; I kind of hinted that the 2 "types" were only separated in hindsight when I used the phrase "...at least as far as their evolutionary import".

I guess the important issue is to what extent such chromosome alterations play a role in such speciation events as the divergence of the human branch from the proto-chimp population. Perhaps we will never know whether it was significant or not...

[mistermack]

The only point where Mack may have a slight point to make is wrt the role of genes in fusion events.......

GenesForLife, I don't think you've even understood my posts.
If you just address posts line by line, without reading any previous context, it's not surprising you get it wrong.

My first comment on this thread was that I doubted that fusion was a block to reproduction initially. Yet you came in pages later and demanded a citation for the exact opposite. You've clearly got what I'm saying backwards.

As far as genes causing fusion is concerned, I made it perfectly clear that I was talking in the context of inheritance, not mechanical mechanism.

For a population to go from unfused to fused chromosomes requires a GENETIC CHANGE in that population, and I argued that that would be unlikely to happen, if fusion was a block to reproduction.
It's in that context that I argued that genes caused fusion.

If you keep reading and replying to single sentences in isolation, you will keep getting it wrong.

[GenesForLife]

The only point where Mack may have a slight point to make is wrt the role of genes in fusion events.......

My first comment on this thread was that I doubted that fusion was a block to reproduction initially. Yet you came in pages later and demanded a citation for the exact opposite. You've clearly got what I'm saying backwards.

In that case, congratulations to you, the evidence I've cited (which you are usually loathe to provide whenever you go on a journey of speculations) suggests that fusion isn't deleterious wrt loss of fertility, firstly, and that this is a prerequisite for fusion events to successfully spread through populations, I have provided apposite citations supporting your speculation.

As far as genes causing fusion is concerned, I made it perfectly clear that I was talking in the context of inheritance, not mechanical mechanism.

Regardless of what context you put it in that sentence is a far-fetched, ill-fitting description, it is almost like claiming life causes death, because it is life that produces organisms that are capable of death.

For a population to go from unfused to fused chromosomes requires a GENETIC CHANGE in that population, and I argued that that would be unlikely to happen, if fusion was a block to reproduction.It's in that context that I argued that genes caused fusion.

Well the evidence is quite clear that fusion is not necessarily a block to reproduction, there is no need for speculation with respect to this, however, the term "genomic change" would be more apt.

[mistermack]

Regardless of what context you put it in that sentence is a far-fetched, ill-fitting description, it is almost like claiming life causes death, because it is life that produces organisms that are capable of death.

Only if you disregard the context. That's my point.
You do disregard the context and take sentences in isolation. That's how you end up arguing with the opposite of what people have said.

Well the evidence is quite clear that fusion is not necessarily a block to reproduction, there is no need for speculation with respect to this, however, the term "genomic change" would be more apt.

Not necessarily. Genomic change comes about as a result of proliferation or extinction of individual genes, and combinations. Genomic change doesn't really get across the point I was making.

Anyway, I can't believe I'm quibbling with you about which word is best.

It doesn't matter, if you read the context. I'm trying to help here, not criticise. If you keep taking stuff out of context, you're going to make a lot of work for yourself in the long run.
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